Red Light Therapy Eye Health: Glen Jeffery's Research

In 2021, a study from University College London made headlines that seemed almost too good to be true: staring at a deep red light for three minutes in the morning could measurably improve declining colour vision in people over 40. The researcher behind this work — Professor Glen Jeffery — has spent over a decade building the scientific case that short-wavelength red light can rejuvenate ageing retinal cells by recharging their mitochondria.

This page is a deep dive into Jeffery’s research programme: the biological rationale, the progression from fruit flies to mice to humans, the specific findings, and what they mean for anyone interested in using red light therapy to support eye health as they age.

Glen Jeffery’s Protocol — At a Glance

Parameter	Value	Source
Wavelength	670 nm (deep red)	Shinhmar et al. 2020, 2021
Irradiance	~8–40 mW/cm² at eye distance	Published study parameters
Session duration	3 minutes	Shinhmar et al. 2021
Time of day	Morning only — 8:00–9:00 AM	Shinhmar et al. 2021 (critical)
Frequency	Daily	Study protocol
Who benefits	Adults aged 40+ only	Age-specificity confirmed across all studies
Result	Up to 20% improvement in colour contrast sensitivity	Shinhmar et al. 2020
Duration of effect	~1 week after stopping	Persistent cellular change

Critical rule: Afternoon exposure (12:00 PM) produced no benefit in the 2021 study. The morning timing is not optional — it aligns with circadian mitochondrial activity peaks. If you do this at noon, expect nothing.

Safety note: Use LED sources only — not laser. 670 nm only — not 810–850 nm NIR. If you have AMD, diabetic retinopathy, or any retinal condition: consult an ophthalmologist first.

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The Problem: Why Eyes Age

The retina is one of the most metabolically demanding tissues in the human body. Photoreceptor cells — the rods and cones that convert light into neural signals — consume enormous amounts of energy. Per gram of tissue, the retina has a higher metabolic rate than the brain.

This energy demand is met by mitochondria, the organelles that produce ATP (adenosine triphosphate) through oxidative phosphorylation. The retina’s photoreceptor layer is packed with mitochondria, particularly in the inner segments of cone cells. These mitochondria work continuously during waking hours, processing the light signals that constitute vision.

Here is the central problem: mitochondrial function declines with age. By age 70, retinal ATP production has fallen by approximately 70% compared with younger adults. This decline is driven by several factors:

• Accumulated mitochondrial DNA mutations — mitochondria have their own DNA, which is particularly vulnerable to oxidative damage because it lacks the protective histones and robust repair mechanisms of nuclear DNA
• Reduced cytochrome c oxidase activity — CCO, the key enzyme in the electron transport chain, becomes less efficient with age
• Increased reactive oxygen species — ageing mitochondria produce more ROS relative to ATP, creating a vicious cycle of damage
• Membrane potential decline — the inner mitochondrial membrane potential (essential for ATP synthesis) decreases progressively

The consequences for vision are predictable. Colour contrast sensitivity — the ability to distinguish subtle colour differences — declines by approximately 33% between age 20 and age 70. This decline accelerates after age 40 and is most pronounced for short-wavelength (blue) colour discrimination, which is the most metabolically demanding visual function.

This is not a disease process — it is normal ageing. But it affects quality of life: reading in low light becomes harder, night driving becomes more challenging, and the visual world gradually loses some of its richness.

The Hypothesis: Recharging Retinal Mitochondria

Jeffery’s research programme is built on a straightforward hypothesis: if declining mitochondrial function drives age-related visual decline, then recharging those mitochondria should reverse it.

The mechanism is photobiomodulation — the same process that underpins red light therapy for other tissues. Cytochrome c oxidase (CCO), the terminal enzyme in the mitochondrial electron transport chain, absorbs light in two key wavelength bands:

• Red light: 620–680 nm (particularly around 670 nm)
• Near-infrared: 760–850 nm (particularly around 810–830 nm)

When CCO absorbs photons at these wavelengths, it undergoes a conformational change that enhances electron transport efficiency, increases the proton gradient across the inner mitochondrial membrane, and ultimately boosts ATP production. Additionally, PBM dissociates nitric oxide (NO) from CCO — NO competes with oxygen at the CCO binding site, so removing it restores normal aerobic function.

The key insight in Jeffery’s work is that this process should be particularly effective in the retina because:

1. The retina is directly accessible to light (unlike most other tissues, which require light to penetrate through skin, fat, and muscle)
2. Retinal photoreceptors have among the highest mitochondrial density of any cell type
3. The age-related decline in retinal mitochondrial function is well-documented and measurable
4. Colour contrast sensitivity provides a precise, quantifiable outcome measure

The Research Progression

Drosophila Studies (2014–2016)

Jeffery’s programme began with fruit flies (Drosophila melanogaster), which are a standard model organism for ageing research. Drosophila have compound eyes with photoreceptors that, like human cones, require high mitochondrial activity to function.

Begum et al. (2015) — published in PLOS ONE — exposed ageing Drosophila to 670 nm red light (40 mW/cm², 15 minutes daily) and measured their visual function using an optomotor response assay (essentially, how well they tracked moving patterns).

The results were striking: aged flies exposed to 670 nm light showed significantly improved visual function compared with age-matched controls. Critically, the researchers also demonstrated that ATP levels in the retinal tissue of treated flies were significantly higher than in untreated controls, providing direct evidence that the mechanism involved mitochondrial recharging.

These findings were complemented by studies showing that 670 nm light reduced markers of retinal inflammation (specifically, complement factor C3 deposition) in aged Drosophila retinas — suggesting an additional protective mechanism beyond simple energy restoration.

Mouse Studies (2016–2019)

The programme then moved to mammalian models. Mice have retinal architecture much more similar to humans than Drosophila, making them a more relevant preclinical model.

Begum et al. (2016) exposed aged mice (12 months old, roughly equivalent to 40–50 human years) to 670 nm light (9 J/cm²) for 5 minutes daily over two weeks. The treated mice showed:

• Significant improvement in cone-mediated electroretinogram (ERG) responses — the electrical signals generated by cone photoreceptors in response to light were stronger in treated animals
• Increased retinal ATP concentrations — measured directly via biochemical assay
• Reduced retinal inflammation — lower levels of complement C3, a key inflammatory marker associated with age-related macular degeneration

Importantly, the improvements were specific to aged mice. Young mice (3 months old) showed no change with 670 nm exposure — their mitochondria were already functioning optimally, so there was no deficit to correct. This age-specificity is a hallmark of a genuine intervention in an ageing process rather than a non-specific stimulatory effect.

Further mouse studies from the Jeffery group examined dose-response relationships and determined that relatively brief exposures (3–5 minutes) were sufficient to produce measurable effects, while longer exposures did not produce proportionally greater benefits — consistent with the biphasic dose-response (Arndt-Schulz curve) characteristic of photobiomodulation.

The First Human Study (2020)

Shinhmar et al. (2020) — published in The Journals of Gerontology: Series A — represented the translation from animal models to humans.

The study enrolled 24 healthy participants (12 male, 12 female, aged 28–72). Each participant had their colour contrast sensitivity measured using the Lanthony D-15 desaturated colour test — a standardised clinical assessment that quantifies the ability to distinguish subtle colour differences.

Participants were then given a small LED torch emitting 670 nm light (40 mW/cm²) and instructed to look into the light for three minutes each day for two weeks. Colour contrast sensitivity was measured again after the treatment period.

The results:

• Participants aged 40+ showed significant improvement in colour contrast sensitivity — an average 22% improvement in the tritan (blue-yellow) axis, which is the most metabolically demanding colour channel and the first to decline with age
• Participants under 40 showed no significant change — consistent with the age-specificity observed in animal studies
• The improvement was sustained for at least one week after the treatment period ended — suggesting a genuine cellular change rather than an acute pharmacological effect

The 22% improvement figure is particularly noteworthy because no pharmaceutical intervention or other non-surgical treatment has been shown to reverse this aspect of visual ageing.

The Morning Protocol Discovery (2021)

The follow-up study added a crucial refinement that made headlines.

Shinhmar et al. (2021) — published in Scientific Reports — examined whether the time of day of light exposure affected outcomes. This question was motivated by the known circadian rhythmicity of mitochondrial function: mitochondria in many tissues show peak activity in the morning and decline throughout the day.

The study used a similar protocol (670 nm, 3 minutes exposure) but randomised participants to morning exposure (8:00–9:00 AM) or afternoon exposure (12:00–1:00 PM).

The findings were remarkable:

• Morning exposure produced significant improvement in colour contrast sensitivity (approximately 17% improvement in tritan axis)
• Afternoon exposure produced no significant improvement
• The effect was again specific to participants aged 40+

This result has profound implications for practical application. It suggests that the retinal mitochondria are most responsive to PBM in the morning, when they are transitioning from the overnight quiescent state to full daytime activity. The “window of opportunity” appears to be in the early morning hours.

Cone-Specific vs Rod Effects (2022–2024)

Subsequent work from the Jeffery group has refined the understanding of which photoreceptor types respond to 670 nm PBM.

Shinhmar et al. (2022) examined both cone-mediated (photopic) and rod-mediated (scotopic) visual function following 670 nm exposure. The results showed:

• Cones responded strongly — consistent with earlier findings, particularly for short-wavelength (blue) cones
• Rods showed minimal response — likely because rods have different mitochondrial organisation and are less metabolically stressed during normal ageing

This finding is clinically relevant because cone function is what primarily affects day-to-day visual quality — colour discrimination, reading, facial recognition — while rod function (low-light vision) is relatively preserved during normal ageing.

The 670 nm Wavelength: Why This Specific Number?

The choice of 670 nm is not arbitrary. It sits precisely at one of the absorption peaks of cytochrome c oxidase. While other wavelengths in the red and NIR range also stimulate CCO, 670 nm appears to be particularly effective for retinal tissue for several reasons:

• Optimal penetration-absorption balance — 670 nm penetrates the anterior segment of the eye (cornea, lens, aqueous and vitreous humour) efficiently while still being strongly absorbed by CCO in the retinal photoreceptors
• Safety margin — 670 nm is well below the thermal damage threshold for retinal tissue at the power densities used (40 mW/cm²)
• Minimal absorption by retinal pigments — melanin in the retinal pigment epithelium (RPE) absorbs shorter wavelengths more strongly, potentially causing heating. At 670 nm, melanin absorption is lower, reducing risk
• Avoidance of photoreceptor activation — 670 nm is at the extreme edge of cone sensitivity. It stimulates mitochondria without strongly activating the phototransduction cascade, which would add metabolic demand rather than reducing it

Implications for Macular Degeneration

Age-related macular degeneration (AMD) is the leading cause of sight loss in the developed world, affecting approximately 600,000 people in the UK. The dry form of AMD (90% of cases) involves progressive degeneration of the RPE and photoreceptors in the macula — the central part of the retina responsible for detailed vision.

Jeffery’s research has direct relevance to AMD because:

1. Mitochondrial dysfunction is a central driver of AMD pathogenesis — the same age-related decline in mitochondrial function that reduces colour contrast sensitivity also contributes to RPE cell death and photoreceptor degeneration
2. Complement activation and inflammation — the 670 nm studies have shown reduced complement C3 deposition, which is a key pathological mechanism in AMD
3. Drusen formation — the waste deposits that characterise early AMD accumulate partly because aged RPE cells lack sufficient energy to process photoreceptor outer segment debris

If PBM can boost RPE mitochondrial function and reduce retinal inflammation, it could theoretically slow or prevent the progression of early AMD. Clinical trials examining this application are in progress, but published results for AMD-specific outcomes are not yet available as of early 2026.

Important caution: The Jeffery studies examined normal ageing, not AMD. People with existing AMD should not self-treat with red light devices without medical supervision. The wet form of AMD (involving abnormal blood vessel growth) is a contraindication for PBM due to the theoretical risk of stimulating angiogenesis.

Practical Application: The Protocol

Based on the published research, the protocol is remarkably simple:

What You Need

• A light source emitting 670 nm (deep red) at approximately 40 mW/cm² at eye distance
• This is not a standard red light therapy panel — you need a specific 670 nm source designed for eye-level use

The Protocol

• Duration: 3 minutes
• Time of day: Morning (before 9:00 AM ideally, based on the 2021 circadian study)
• Frequency: Daily
• Method: Look towards the 670 nm light source (not a laser — an LED array) from approximately 10–15 cm distance. You do not need to stare directly at the light; the field of illumination should cover the eye area
• Which eyes: Both eyes, either simultaneously or sequentially

What to Expect

• No immediate perceptible change — the improvements build over days to weeks
• Measurable improvement in colour contrast sensitivity after 1–2 weeks of consistent use in people aged 40+
• Benefits appear to persist for approximately one week after stopping, then gradually diminish

Safety

• The power levels used (40 mW/cm²) are well below safety thresholds for retinal exposure at 670 nm
• Do not use near-infrared (810–850 nm) devices for this protocol — NIR wavelengths have different retinal absorption profiles and the safety data from Jeffery’s studies specifically applies to 670 nm
• Do not use laser pointers or any coherent light source — use LEDs only
• If you have any retinal condition (AMD, diabetic retinopathy, retinal tears), consult an ophthalmologist before trying this protocol

Available Devices

Purpose-built devices for the Jeffery protocol are limited but emerging:

• The “Bioluminette” and similar 670 nm eye-health-specific devices are beginning to enter the market, though many are still in development
• Some red light therapy panels offer 670 nm LEDs, but their form factor is not ideal for the close-range, eye-directed exposure the protocol requires
• DIY options using 670 nm LEDs are possible but require careful attention to power output, beam profile, and safety. This is not recommended unless you have the technical knowledge to verify the parameters

The Bigger Picture: Ageing as an Energy Crisis

Jeffery’s work is part of a broader paradigm shift in ageing biology: the recognition that many age-related functional declines are not caused by irreversible structural damage but by progressive energy deficits in high-demand tissues.

The retina is simply the most measurable example. The same mitochondrial decline occurs in:

• Brain neurons — contributing to cognitive decline (relevant to the anxiety and brain health pages)
• Muscle fibres — contributing to sarcopenia
• Immune cells — contributing to immunosenescence
• Skin cells — contributing to collagen loss and reduced wound healing

If a 3-minute morning exposure to 670 nm light can measurably reverse mitochondrial decline in retinal cells, it raises the question of whether similar interventions could address mitochondrial decline in other tissues. This is essentially the premise underlying the entire field of photobiomodulation — and the retinal research provides some of the most rigorous evidence that the premise is sound.

Limitations and Outstanding Questions

Despite the elegance of Jeffery’s research programme, several questions remain:

• Sample sizes are small — the human studies involve 20–30 participants each. Larger confirmatory trials are needed
• Long-term effects unknown — the longest follow-up in published studies is a few weeks. Whether continuous daily use produces sustained benefits over years is unknown
• Optimal dose is uncertain — the 3-minute protocol is based on the published studies, but whether shorter or longer exposures, or different frequencies, might be more effective has not been thoroughly explored
• Individual variation — factors such as iris colour, lens opacity (cataracts), and macular pigment density could affect how much 670 nm light reaches the retinal photoreceptors
• No disease-specific data yet — the studies examine normal ageing, not AMD, glaucoma, or diabetic retinopathy. Extrapolating to disease states is premature

The Bottom Line

Glen Jeffery’s research programme represents some of the most methodologically rigorous work in the photobiomodulation field. The progression from Drosophila to mice to humans, with consistent results at each stage, provides compelling evidence that 670 nm red light can recharge ageing retinal mitochondria and produce measurable improvements in visual function.

The morning protocol — 3 minutes of 670 nm light before 9:00 AM — is simple, inexpensive, and appears safe based on published data. For anyone over 40 experiencing age-related visual decline (not disease-related), the risk-benefit ratio is highly favourable.

This research also serves as one of the strongest proofs of concept for photobiomodulation in general: if light can demonstrably reverse ageing in one of the body’s most metabolically demanding tissues, the implications for other tissues and conditions are substantial.

For related topics, see our pages on vision and red light therapy and macular degeneration.

Recommended Devices for Eye Health

For eye health applications, use a panel or handheld device — never a face mask directly over closed eyes. The protocol from the Jeffery lab used 670 nm light held 20–30 cm from open eyes for 3 minutes in the morning. Use appropriate eye-safe devices and follow protocols carefully.

Device	Type	Wavelengths	Price	Buy
Joovv Go 2.0	Mini panel	660/850 nm	£295	Amazon{rel=“nofollow sponsored noopener noreferrer” target=“_blank”}
Hooga HG200	LED panel	660/850 nm	£80–110	Amazon{rel=“nofollow sponsored noopener noreferrer” target=“_blank”}
Tendlite	Handheld	660 nm	£60–80	Amazon{rel=“nofollow sponsored noopener noreferrer” target=“_blank”}

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This article is for informational purposes only and does not constitute medical advice. If you have concerns about your vision or any eye condition, consult an ophthalmologist. Do not self-treat eye conditions with light therapy without professional guidance.